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Signalling Pathways in The Regulation of Cellular Responses to Exercise
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Anders Gudiksen, Stine Ringholm, Henriette Pilegaard
p38 has been shown to directly phosphorylate three different serine residues on PGC-1α, increasing PGC-1α activity in vitro (2), as well as to phosphorylate activating transcription factor 2 (ATF2) and MEF2, thus also promoting PGC-1α transcription (2, 76). ATF2 is a member of the CREB/ATF family of transcription factors that binds to the PGC-1α promoter and induces its transcription (Figure 8.2). Prolonged exercise (marathon running) has been shown to increase p38 and ERK1/2 phosphorylation together with enhancing DNA binding of MEF2 in human SkM (137). Moreover, it has been demonstrated that binding of ATF2 and MEF2 to PGC-1α increases 3 hours into recovery from an exercise bout (107), which may lead to transcription of genes encoding oxidative proteins (22, 105). In addition, MEF2 associated with HDAC5 decreased (indicating a nuclear export of HDAC5 and increased transcription) and MEF2 associated with PGC-1α increased in human SkM in response to 1 hour of moderate-intensity exercise (76) (Figure 8.2). Taken together, this establishes a firm connection between exercise-induced p38 regulation and regulation of mitochondrial biogenesis (Figure 8.2).
Articular Cartilage Development
Published in Kyriacos A. Athanasiou, Eric M. Darling, Grayson D. DuRaine, Jerry C. Hu, A. Hari Reddi, Articular Cartilage, 2017
Kyriacos A. Athanasiou, Eric M. Darling, Grayson D. DuRaine, Jerry C. Hu, A. Hari Reddi
The JNK pathway components are composed of a variety of MAP3Ks (MEKK1-4, MLK1-3, DLK, Tp12, ASK1 and 2, TAO1 and 2, and TAK1) (Weston and Davis 2002). Downstream, the MAPKKs (MKK4 and 7) phosphorylate the dual Thr and Tyr of the three JNK genes, of which 10 isoforms exist. Activated JNK is able to phosphorylate multiple transcription factors, including ATF2, NF-ATc1, HSF01, Stat3, and c-Jun. Of these transcription factors, c-Jun is the best known, and phosphorylation of Ser63 and 73 leads to increased transcription of c-Jun targets. Pharmacological inhibition of JNK can be accomplished by the use of SP600125 (Bennett et al. 2001). Interestingly, JNK plays a limited role in chondrogenesis. JNK is unresponsive to GDF5 treatment, and the phosphorylation state of JNK does not change during chondrogenesis (Nakamura et al. 1999).
Molecular mechanism of miR-204 regulates proliferation, apoptosis and autophagy of cervical cancer cells by targeting ATF2
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Nan Li, XiaoRong Guo, Lei Liu, Lu Wang, Rongjie Cheng
Activating transcription factor 2 (ATF2) belongs to the alkaline leucine zipper transcription factor family. ATF2 is localized on human chromosome 2q32, plays an inhibitory or promoting role in tumours and participates in cell stress, DNA damage and other processes [21]. Activation of ATF2 is mainly through phosphorylation modification after stress stimulation. Phosphorylated ATF2 binds to specific sequence of promoter region of target gene such as cell cycle molecule, adhesion molecule and apoptosis-related molecule, thereby activating target gene expression. Wu et al. [22] found that ATF2 in renal cell carcinoma can regulate the expression of cell cycle protein B1, cell cycle protein D1, vimentin expression, thereby regulating cell proliferation and metastasis. In addition, previous studies [23] have confirmed that miR-204 can specifically inhibit the expression of ATF2 protein and regulate the proliferation, migration and invasion of human brain keratinocytoma tumour cells. In this study, after transfecting ATF2 siRNA into C33A cells, the expression level of autophagy-related protein LC3I/II was significantly decreased (p < .05), cell viability decreased (p < .05) and apoptosis rate increased (p < .05). When miR-204 mimics and ATF2 siRNA were co-transfected into C33A cells, the inhibitory effect of miR-204 on proliferation and autophagy of C33A cells and its promotion of apoptosis were attenuated.
Combination of tetrandrine and 3-n-butylphthalide protects against cerebral ischemia-reperfusion injury via ATF2/TLR4 pathway
Published in Immunopharmacology and Immunotoxicology, 2021
Cunfang Li, Aijun Chai, Yongchao Gao, Xuan Qi, Xuguang Zheng
Activator transcription factor 2 (ATF2) belongs to ATF/CREB transcription factor family and is an important component of activator protein transcription complex [5]. ATF2 binds to toll-like receptor 4 (TLR4) [6]. TLR4 plays a crucial role in the inflammatory response by coupling with a broad range of ligands, which induce the downstream signaling, that is, nuclear factor kappa B (NF-κB) and the release of inflammatory cytokines [7]. NF-κB signaling is involved in immune defense, inflammation, blood production, cell proliferation, and anti-apoptosis [8]. The activation of this signaling pathway promotes neuroinflammatory responses and I/R injury [9]. Therefore, to the ATF2/TLR4 signaling pathway might provide a novel therapeutic strategy in treating brain I/R injury.